This invention relates to systems and methods for reducing the volume of the left or right ventricles of the heart, thereby to facilitate treatment of congestive heart failure, ventricular aneurysms or other related conditions.
A spectrum of disease processes may affect the pumping capability of the heart, impairing its ability to provide adequate circulation for the metabolic needs of the tissues and organs of the body. Diseases specific to the heart include those that 1) interfere with the electrophysiological conduction to the heart; 2) interfere with the inflow or outflow of blood through a heart valve; or 3) affect the myocardium itself, whether by ischemic damage or intrinsic cardiomyopathy. Certain conditions may be improved by medical or surgical interventions, so that the heart is able to pump what the body requires. A conduction problem can be corrected, for example, by a pacemaker. An abnormal heart valve may be replaced.
Unfortunately, lesions of the cardiac muscle itself are more difficult, if not impossible, to repair at present. Techniques involving muscle regeneration by stem cells, for example, do not yet permit reliable restoration of functional myocardium. Instead, when the myocardium is injured, muscle cells that die are typically replaced with non-contractile scar tissue, and muscle cells that have been sublethally damaged may not contract normally. As a result, the heart may lose its ability to pump adequately. Impairment of the heart's contractile capability, if sufficiently severe or advanced, may result in diminished cardiac output (so-called forward failure), damming up of venous return (so-called backward failure), or both. These end results collectively form part of the syndrome of congestive heart failure (CHF).
Other CHF signs and symptoms are caused by the body's attempt to compensate for inadequate cardiac pumping. When the heart is not pumping enough blood to meet the body's demands, the body activates a number of compensatory physiologic mechanisms. If these physiological mechanisms are ineffective to restore adequate circulation, or if they become overextended, they no longer permit compensation. Instead, the system decompensates and may tip over into CHF.
Understanding the pathophysiology of CHF therefore involves understanding the compensatory mechanisms by which the heart responds to a mismatch between the body's metabolic needs and the heart's pumping capabilities. These compensatory mechanisms include: 1) the Frank-Starling mechanism, by which preload is increased to enhance cardiac performance; 2) myocardial hypertrophy, with an increase of contractile cell mass; 3) cardiac chamber dilation; and 4) neurohumoral adaptation, including the activation of the renin-angiotensin-aldosterone system and the release of norepinephrine. Under normal circumstances, these mechanisms work together to meet increased circulatory demands during exercise, stress or fever. When the demand on these adaptive mechanisms is too great, perhaps because of excessive metabolic requirements or inadequate pumping capability, the adaptive mechanisms themselves become maladaptive.
Under normal conditions, the heart responds to increasing demands by augmenting preload, increasing the heart rate, and increasing the contractility of the ventricles. An increase in preload leads to an increased stretch of the myocardial fibers. As a result, the force of the next cardiac contraction is increased, as described by the Frank-Starling curve. According to the Frank-Starling mechanism, the more the heart fills during diastole, the greater the force of contraction during the next systole. With overfilling of the heart, however, the cardiac muscle fibers become overstretched and this mechanism becomes ineffective. After a certain degree of stretch, the fibers no longer respond to increasing stretch by increasing contractility. Instead, their contractility diminishes. The overstretched heart becomes less able to pump, and the ventricles may dilate.
Over a longer period of time, cardiac muscle responds to increasing work demands by increasing in size, just like skeletal muscle. The cardiac muscle cells cannot increase in number, but can only increase in size. This mechanism is called hypertrophy. With myocardial hypertrophy, the ventricular wall thickness may increase and the ventricle may enlarge as the myocardial fibers elongate. The myocardial cell proteins formed during hypertrophy may be abnormal, however, which may affect their functional efficacy. Hypertrophy may also increase the myocardium's metabolic demands, such that these demands outstrip the circulatory supply.
Other cardiac compensatory mechanisms, such as increases in heart rate and contractility that are brought about by norepinephrine stimulation may exacerbate functional decompensation of the heart, because the metabolic needs of the cardiac muscle may increase beyond the circulation's ability to satisfy them. In addition, non-cardiac compensatory mechanisms set in motion by decreased cardiac output or contractility may also have adverse effects on myocardial function. For example, as the body compensates for decreased cardiac output by retaining sodium and water, there may be increased ventricular distention and a subsequent decrease in contractile efficiency. The body may respond by an additional increase in heart rate, increasing the myocardium's metabolic demands even further.
Where the compensatory mechanisms have lost their ability to improve cardiac performance appropriately or when the patient shows symptoms derived from the compensatory mechanisms or the underlying cardiac performance problem, medical intervention is warranted. Pharmacological treatment for CHF generally endeavors to increase myocardial contractility or to affect the now-dysfunctional compensation mechanisms. Three general classes of drugs have been found useful: 1) inotropic agents, which increase the strength of cardiac muscle contraction; 2) vasodilators, which decrease the resistance and head of pressure against which the heart must pump; and 3) diuretic agents, which counteract fluid retention and preload.
The New York Heart Association has proposed a useful functional classification system for CHF. Class I patients are not limited by cardiac symptoms and may engage in normal physical activity. Class II patients suffer symptoms like fatigue or dyspnea during ordinary physical activity. Class III patients experience a significant limitation of normal physical activities. Class IV patients suffer symptoms at rest or with any physical exertion. Pharmacological intervention may improve a patient's cardiac status sufficiently so that the person may enjoy an acceptable quality of life.
CHF, however, is accompanied by a grim prognosis. CHF patients may require multiple hospital admissions for management, and may deteriorate despite aggressive medical management. The majority of CHF patients may die within several years of diagnosis. NYHA Class IV patients may experience a 65% one-year mortality.
Heart transplantation has assumed a central role in the treatment of advanced CHF in certain patients. Transplantation, however, is a limited option, because of the restricted supply of donor organs and the need for immunosuppression. Nearly 5 million patients in the U.S. suffer from CHF. Approximately 500,000 patients are newly diagnosed each year. Yet fewer than 3,000 heart transplants are performed for this condition annually in the U.S., well below the number required to treat severely afflicted patients.
Standard surgical procedures such as coronary revascularization and mitral valve replacement are understood to be beneficial for certain CHF patients. Reconstruction of the mitral subvalvular apparatus may also improve left ventricular function in CHF patients. Implantable ventricular assist devices may provide temporary cardiac output support for CHF patients. A variety of surgical techniques permit reconstruction of the left ventricle itself, for example to treat a dyskinetic aneurysm or an akinetic segment following infarction. Partial left ventriculectomy may also involve excising viable but hypocontractile myocardium, to permit remodeling of the overstretched left ventricle. Dynamic cardiomyoplasty uses the patient's own skeletal muscle (e.g., the latissimus dorsi) to assist the heart in pumping and/or to decrease the stress on the myocardial wall. Passive ventricular constraint devices have been developed to improve cardiac function. For example, the Acorn CorCap™ offers flexible external constraint. In addition, devices may be positioned within the heart to constrain the size and/or shape of the ventricle.
There remains a need in the art for a treatment modality for CHF that helps to improve the anatomy and physiology of the failing left ventricle. A need also exists for a CHF treatment device that is adjustable once applied to the left ventricle, so that it can more closely adapt to the anatomic and physiological needs of the patient. Furthermore, there is a need for a device that is implantable using minimally invasive or catheter-based techniques in severely compromised CHF patients.